"Only 2 of the 29 meta-analyses even mentioned the issue of who funded the original drug trials, and even those 2 did it in very obscure places in the published articles," said Thombs, a psychologist and assistant professor in the Department of Psychiatry at McGill University. "Not one of the meta-analyses mentioned whether researchers who conducted the trials were employed by industry or personally received money from industry."

In addition,

The team identified 7 meta-analyses where every single drug trial included was paid for, at least in part, by the maker of the drug or had investigators linked financially to drug makers. In 6 of the 7 meta-analyses, however, there was no mention of who funded the drug trials.

2. Actos seems to cause an increased risk of bladder cancer in those who take it for two years or more. Note the weaselly way that this result is reported. The definition of those "taking Actos" included people who only filled two prescriptions--i.e. the many who dropped it because of cost, ineffectiveness, and side effects. Among those who continued taking the drug cancer was more prevalent. Who do you think funded this study? You'll never know because the ADA's Diabetes Care's abstracts don't reveal the study's sponsorship.

A Kaiser study that controlled for a huge number of variables (possibly making the statistical results meaningless) found an elevated risk of melanoma among those who took Actos but downplayed this finding in the study's conclusion. Funding of this study is unknown.

3. Actos has a huge impact on preventing the progress to diabetes (i.e. blood sugar levels defined as "diabetic" on a fasting glucose or glucose tolerance test.) This is a high profile study published in the New England Journal of Medicine that got a ton of coveraage. To their credit, the NEJM, in its abstract, identifies the sponsor of this study--the makers of Actos. The drawbacks the study found were that Actos "was associated with significant weight gain and edema."

What is missing here is the information that other studies have found that exercise and dietary changes can produce a very similar decrease in progress to diabetes without any side effects and without Actos' risk of heart failure, macular edema (which can cause blindness)and permanent weight gain.

All animals except people have a gene, Virtually all mammals produce specific sugar molecules that aid cells in interacting with their environment. That is, all except humans. Around 2 to 3 million years ago humans lost CMAH, a gene that codes for an enzyme that produces the sugar Neu5Gc.

To test the role of this gene, researchers compared two sets of mice. One group had a normal CMAH function and Neu5Gc production, the other group did not—just like humans. Both groups of mice were fed a diet that normally induces obesity and insulin resistance (metabolic syndrome), and both groups experienced these symptoms. However, only the mice missing the CMAH gene had lost the ability to produce insulin in the pancreas.

There are many other differences between mice and humans that make them a poor model for type 2 diabetes--most notably, the fact that most mice fed high fat diets develop diabetes while humans (for example, Inuit) fed the same diet do not.

2. Gut bacteria can control organ functions in mice--including liver glucose levels. What's interesting here is that we know there is an association between gut bacteria and obesity in humans, so it is possible this mouse finding is relevant. Are the trace amounts of antibiotics, pesticides and herbicides that are in our food and water supply changing our gut flora in ways that promote the growth of bacteria that contribute to diabetes?

1. Strong evidence that antidepressants are causing thickening of carotid arteries (strongly associated with heart attacks). This study was presented at 2011 American College of Cardiology annual scientific session, New Orleans, and received NO play in the press--note that it is Business Week who picked up on it. This was an identical twin study where one twin was taking antidepressants and the other wasn't. The study authors found that "a twin taking an antidepressant had a greater intima-media thickness than a brother not taking the drugs." Given that SSRIs greatly increase insulin resistance this shouldn't be a shocker. Don't expect to hear any more about this as drug companies spend even MORE money marketing antidepressants than they do dangerous diabetes drugs and their advertising--and research--dollars affect media coverage.

All the other sulfonylurea drugs raised the risk of death, whether or not people had had a heart attack before taking them. The study concludes: "Monotherapy with the most used ISs, including glimepiride, glibenclamide, glipizide, and tolbutamide, seems to be associated with increased mortality and cardiovascular risk compared with metformin. Gliclazide and repaglinide appear to be associated with a lower risk than other I[nsulin]S[ecretagogues]s."

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I was diagnosed with diabetes in 1998. Since then I've kept my A1cs in the 5.0-6.0% range using the techniques you'll find explained at The main Blood Sugar 101 Web Site, where you'll also find extensive discussion of the peer-reviewed research that backs up the statements you read here.

I've also published two books on related subjects, Blood Sugar 101: What They Don't Tell You About Diabetes, which was an Amazon Diabetes bestseller for 3 years and Diet 101: The Truth About Low Carb Diets.